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吉兰-巴雷综合征源空肠弯曲菌致急性周围神经病Hartley豚鼠模型初步建立
引用本文:李世平,杨静,徐飞,杜风萍,李震中. 吉兰-巴雷综合征源空肠弯曲菌致急性周围神经病Hartley豚鼠模型初步建立[J]. 临床荟萃, 2014, 0(8): 896-899
作者姓名:李世平  杨静  徐飞  杜风萍  李震中
作者单位:李世平(河北医科大学第二医院 神经内科 河北省神经病学重点实验室 河北省心脑血管研究所,河北 石家庄,050000);杨静(河北医科大学第二医院 神经内科 河北省神经病学重点实验室 河北省心脑血管研究所,河北 石家庄,050000);徐飞(河北医科大学第二医院 神经内科 河北省神经病学重点实验室 河北省心脑血管研究所,河北 石家庄,050000);杜风萍(河北医科大学第二医院 神经内科 河北省神经病学重点实验室 河北省心脑血管研究所,河北 石家庄,050000);李震中(河北医科大学第二医院 神经内科 河北省神经病学重点实验室 河北省心脑血管研究所,河北 石家庄,050000);
基金项目:国家自然科学基金资助项目(项目编号:81072481,30471919)863计划资助项目(项目编号:2006AA02A237)
摘    要:
目的初步建立吉兰-巴雷综合征(Guilliain-Barre syndrome,GBS)源空肠弯曲菌感染致急性周围神经病Hartley豚鼠模型。方法以GBS患者分离的空肠弯曲菌经微需氧培养后制备菌悬液灌喂豚鼠。自灌喂当日起每日观察豚鼠的临床症状并分别对出现肢体活动障碍及灌胃后2周、3周、4周、5周的豚鼠进行取材,取脊神经根、坐骨神经及臂丛神经,进行苏木精-伊红染色(HE染色)、锇酸染色、免疫组织化学进行神经病理观察。结果空肠弯曲菌自然感染豚鼠后,豚鼠于5周内出现活动减少,食欲减退,体质量减轻症状;分别于2周、3周、4周出现神经病理改变,表现为HE染色可见神经纤维结构多样,轴索肿胀。免疫组织化学染色:鼠抗人神经细丝蛋白单克隆抗体示神经丝粗细不等,节段性萎缩;兔抗人髓磷脂碱性蛋白:髓鞘厚度均一,未见脱髓鞘样改变。锇酸染色:可见神经皱缩、髓鞘塌陷。结论吉兰-巴雷综合征源空肠弯曲菌口服灌喂感染Hartley豚鼠可导致急性周围神经病;Hartley豚鼠可以作为GBS的研究模型动物。

关 键 词:格林-巴利综合征  空肠弯曲杆菌  周围神经系统疾病  豚鼠

Establishment of the model of Hartley guinea pigs with peripheral nerve disease induced by Guilliain-Barre syndrome campylobacter jejuni
LI Shi-ping;YANG Jing;XU Fei;DU Feng-ping;LI Zhen-zhong. Establishment of the model of Hartley guinea pigs with peripheral nerve disease induced by Guilliain-Barre syndrome campylobacter jejuni[J]. Clinical Focus, 2014, 0(8): 896-899
Authors:LI Shi-ping  YANG Jing  XU Fei  DU Feng-ping  LI Zhen-zhong
Affiliation:LI Shi-ping;YANG Jing;XU Fei;DU Feng-ping;LI Zhen-zhong;(Department of Neurology,the Second Hospital of Hebei Medical University,Key Laboratory of Neurology in Hebei Province,Cardiovascular and Cerebrovascular Research Institute of Hebei Province; Sh ij iazhuan g 050000, China)
Abstract:
Objective To establish the model of Hartley guinea pigs with peripheral nerve disease induced by Guillain-Barre syndrome(GBS)-campylobacter jejuni.Methods Campylobacter jejuni isolated from the feces of GBS patients were fed guinea pigs after being micro-aerobic cultured.Since that day,the clinical symptoms of guinea pigs were observed daily,and guinea pigs with the limb movement disorder and gavage for 2weeks,3weeks,4weeks,5weeks were collected,in which the collected root of spinal nerves,sciatic nerve and brachial plexus were pathologically observed in hematoxylin eosin staining(HE staining),osmic acid staining and immunohistochemistry.Results The guinea pigs naturally infected with Campylobacter jejuni had symptoms of less activity,decreased appetite and body mass loss;the guinea pigs had nerve pathological changes for 2week,3weeks,4weeks,which manifested as the diversity of nerve fiber structure and swelling of axon with HE staining.Immunohistochemical staining with mouse anti human neurofilament monoclonal antibody of neurofilament showed different thickness and segmental atrophy;rabbit anti human myelin basic protein showed uniformity of myelin sheath thickness,but there was no demyelination.Osmic acid staining showed that the nerve was shrinking and myelin was collapsed.Conclusion The oral feeding of GBScampylobacter jejuni to Hartley guinea pigs could cause acute peripheral neuropathy syndrome;Hartley guinea pig can be used as animal model for the study of GBS.
Keywords:Guillain-Barre syndrome  campylobacter jejuni  peripheral nervous system diseases  guinea pigs
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